scholarly journals Lifestyle Factors, Mitochondrial Dynamics, and Neuroprotection

2020 ◽  
Author(s):  
Katheryn Broman ◽  
Abigail U. Davis ◽  
Jordan May ◽  
Han-A Park
Keyword(s):  
Molecular Dynamics ◽  
Energy Consumption ◽  
Mitochondrial Dynamics ◽  
Lifestyle Factors ◽  
Brain Cells ◽  
Pathological Conditions ◽  
Promising Target ◽  
Translational Approach ◽  
Intracellular Energy ◽  
The Brain

The brain requires vast amounts of energy to carry out neurotransmission; indeed, it is responsible for approximately one-fifth of the body’s energy consumption. Therefore, in order to understand functions of brain cells under both normal and pathological conditions, it is critical to elucidate dynamics of intracellular energy. The mitochondrion is the key intercellular organelle that controls neuronal energy and survival. Numerous studies have reported a correlation between altered mitochondrial function and brain-associated diseases; thus mitochondria may serve as a promising target for treating these conditions. In this chapter, we will discuss the mechanisms of mitochondrial production, movement, and degradation in order to understand accessibility of energy during physiological and pathological conditions of the brain. While research targeting molecular dynamics is promising, translation into clinical relevance based on bench research is challenging. For these reasons, we will also summarize lifestyle factors, including interventions and chronic comorbidities that disrupt mitochondrial dynamics. By determining lifestyle factors that are readily accessible, we can propose a new viewpoint for a synergistic and translational approach for neuroprotection.

A Microscopic Demonstration of the Normal and Pathological Histology of Mesoglia Cells

1900 ◽  
Vol 46 (195) ◽  
pp. 724-724 ◽  
Author(s):  
Ford Robertson
Keyword(s):  
Cell Body ◽  
Brain Structure ◽  
Grey Matter ◽  
Brain Cells ◽  
Nerve Fibres ◽  
Pathological Conditions ◽  
Exact Function ◽  
Microscopic Demonstration ◽  
A Cell ◽  
The Brain

Dr. Clouston in the unavoidable absence of Dr. Ford Robertson made the following remarks:—The first fact that I have to direct the attention of the meeting to is that Dr. Ford Robertson has devised a new method of examining nerve-tissues by depositing platinum in them. By the use of this platinum method he has demonstrated, amongst other things, that what is called the neuroglia is composed of two sets of elements instead of one, as is generally considered. The neuroglia, as exhibited by this and other methods, is attached to the arteries, to the fibres, and to the brain-cells, forming a generally supporting medium. Dr. Robertson has discovered that in addition to this there is another set of cells, which he has called the mesoglia cells, consisting in a typical form of a cell-body, a nucleus and a number of processes. These processes are in no way connected either with the vascular substance or with the nerve-cells or the nerve-fibres. The mesoglia cells are entirely different from neuroglia cells in appearance, and are found in both the white and grey matter, and in such abundance that Dr. Robertson thinks that there are as many mesoglia cells as there are neuroglia cells existing all through the brain. Sometimes they have no processes, sometimes two processes, but the illustrations show a typical mesoglia cell from the dog and from man. The exact function of these mesoglia cells we certainly do not know, but they certainly do not act in any way as a support to the general brain structure. The mesoglia cells seem to have a phagocyte action in certain pathological conditions. They supply, if not all, at least the greater part of the amyloid bodies which are found in some of the chronic brain degenerations. I think you will agree that it is very important that Dr. Ford Robertson should have discovered a new element in the brain, the particular use of which will doubtless be demonstrated by some of the large number of enthusiastic workers on this subject.

Energy Metabolism and Effects of Energy Depletion or Exposure to Glutamate

1992 ◽  
Vol 70 (S1) ◽  
pp. S107-S112 ◽  
Author(s):  
Louis Sokoloff
Keyword(s):  
Energy Metabolism ◽  
Brain Cells ◽  
Cerebral Hypoxia ◽  
Energy Depletion ◽  
Pathological Conditions ◽  
Oxidative Energy Metabolism ◽  
The Subject ◽  
Tissue Acidosis ◽  
The Brain

The entire program of the first day of the IBRO satellite meeting entitled Ions, Water, and Energy in Brain Cells was devoted to the subject of energy. There were three sessions on the topics of energy metabolism, activation, and development and pathological conditions, followed by a final general discussion on the contents of the day's topics. During this general discussion there were spirited exchanges on the role of glycogen in the energy metabolism of the brain, on the metabolic source of the energy consumed by functional activity, e.g., glycolytic or oxidative energy metabolism, and on the sources of the acid-equivalents that are responsible for the tissue acidosis accompanying cerebral hypoxia. Despite the arguments pro and con presented on all of the issues that were discussed, it is doubtful that a consensus was achieved on most of the issues.Key words: glycogen, glycolysis, oxidative metabolism, acidosis, energy metabolism.

Presence of antibody in virus-infected brain cells of SSPE ferrets

1983 ◽  
Vol 41 ◽  
pp. 804-805
Author(s):  
Hannah R. Brown ◽  
Tammy L. Donato ◽  
Halldor Thormar
Keyword(s):  
Measles Virus ◽  
Plasma Cells ◽  
Subacute Sclerosing Panencephalitis ◽  
Protein A ◽  
Neutralizing Antibody ◽  
Brain Cells ◽  
Antibody Titers ◽  
A Cell ◽  
The Central Nervous System ◽  
The Brain

Measles virus specific immunoglobulin G (IgG) has been found in the brains of patients with subacute sclerosing panencephalitis (SSPE), a slowly progressing disease of the central nervous system (CNS) in children. IgG/albumin ratios indicate that the antibodies are synthesized within the CNS. Using the ferret as an animal model to study the disease, we have been attempting to localize the Ig's in the brains of animals inoculated with a cell associated strain of SSPE. In an earlier report, preliminary results using Protein A conjugated to horseradish peroxidase (PrAPx) (Dynatech Diagnostics Inc., South Windham, ME.) to detect antibodies revealed the presence of immunoglobulin mainly in antibody-producing plasma cells in inflammatory lesions and not in infected brain cells.In the present experiment we studied the brain of an SSPE ferret with neutralizing antibody titers of 1:1024 in serum and 1:512 in CSF at time of sacrifice 7 months after i.c. inoculation with SSPE measles virus-infected cells. The animal was perfused with saline and portions of the brain and spinal cord were immersed in periodate-lysine-paraformaldehyde (P-L-P) fixative. The ferret was not perfused with fixative because parts of the brain were used for virus isolation.

scholarly journals When the Balance Tips: Dysregulation of Mitochondrial Dynamics as a Culprit in Disease

2021 ◽  
Vol 22 (9) ◽  
pp. 4617
Author(s):  
Styliana Kyriakoudi ◽  
Anthi Drousiotou ◽  
Petros P. Petrou
Keyword(s):  
Insulin Resistance ◽  
Mitochondrial Function ◽  
Human Disease ◽  
Molecular Mechanisms ◽  
Mitochondrial Dynamics ◽  
Mitochondrial Fusion ◽  
Mitochondrial Morphology ◽  
Disease Development ◽  
Pathological Conditions ◽  
Wide Range

Mitochondria are dynamic organelles, the morphology of which is tightly linked to their functions. The interplay between the coordinated events of fusion and fission that are collectively described as mitochondrial dynamics regulates mitochondrial morphology and adjusts mitochondrial function. Over the last few years, accruing evidence established a connection between dysregulated mitochondrial dynamics and disease development and progression. Defects in key components of the machinery mediating mitochondrial fusion and fission have been linked to a wide range of pathological conditions, such as insulin resistance and obesity, neurodegenerative diseases and cancer. Here, we provide an update on the molecular mechanisms promoting mitochondrial fusion and fission in mammals and discuss the emerging association of disturbed mitochondrial dynamics with human disease.

scholarly journals Clobetasol promotes neuromuscular plasticity in mice after motoneuronal loss via sonic hedgehog signaling, immunomodulation and metabolic rebalancing

2021 ◽  
Vol 12 (7) ◽  
Author(s):  
Nunzio Vicario ◽  
Federica M. Spitale ◽  
Daniele Tibullo ◽  
Cesarina Giallongo ◽  
Angela M. Amorini ◽  
...  
Keyword(s):  
Sonic Hedgehog ◽  
Hedgehog Signaling ◽  
Neural Regeneration ◽  
Metabolic Effects ◽  
Motor Impairments ◽  
Sonic Hedgehog Signaling ◽  
Neuroprotective Effects ◽  
Promising Target ◽  
Translational Approach ◽  
Lateral Sclerosis

AbstractMotoneuronal loss is the main feature of amyotrophic lateral sclerosis, although pathogenesis is extremely complex involving both neural and muscle cells. In order to translationally engage the sonic hedgehog pathway, which is a promising target for neural regeneration, recent studies have reported on the neuroprotective effects of clobetasol, an FDA-approved glucocorticoid, able to activate this pathway via smoothened. Herein we sought to examine functional, cellular, and metabolic effects of clobetasol in a neurotoxic mouse model of spinal motoneuronal loss. We found that clobetasol reduces muscle denervation and motor impairments in part by restoring sonic hedgehog signaling and supporting spinal plasticity. These effects were coupled with reduced pro-inflammatory microglia and reactive astrogliosis, reduced muscle atrophy, and support of mitochondrial integrity and metabolism. Our results suggest that clobetasol stimulates a series of compensatory processes and therefore represents a translational approach for intractable denervating and neurodegenerative disorders.

scholarly journals Effect of Water and Ethanol Extracts from Hericium erinaceus Solid-State Fermented Wheat Product on the Protection and Repair of Brain Cells in Zebrafish Embryos

Molecules ◽  
2021 ◽  
Vol 26 (11) ◽  
pp. 3297
Author(s):  
Shun-Kuo Sun ◽  
Chun-Yi Ho ◽  
Wei-Yang Yen ◽  
Su-Der Chen
Keyword(s):  
Solid State ◽  
Brain Cell ◽  
Hot Water ◽  
Raw Material ◽  
Brain Cells ◽  
Zebrafish Embryos ◽  
Hericium Erinaceus ◽  
Water Extracts ◽  
The Brain ◽  
Wheat Product

Extracts from Hericium erinaceus can cause neural cells to produce nerve growth factor (NGF) and protect against neuron death. The objective of this study was to evaluate the effects of ethanol and hot water extracts from H. erinaceus solid-state fermented wheat product on the brain cells of zebrafish embryos in both pre-dosing protection mode and post-dosing repair mode. The results showed that 1% ethanol could effectively promote zebrafish embryo brain cell death. Both 200 ppm of ethanol and water extracts from H. erinaceus solid-state fermented wheat product protected brain cells and significantly reduced the death of brain cells caused by 1% ethanol treatment in zebrafish. Moreover, the zebrafish embryos were immersed in 1% ethanol for 4 h to cause brain cell damage and were then transferred and soaked in the 200 ppm of ethanol and water extracts from H. erinaceus solid-state fermented wheat product to restore the brain cells damaged by the 1% ethanol. However, the 200 ppm extracts from the unfermented wheat medium had no protective and repairing effects. Moreover, 200 ppm of ethanol and water extracts from H. erinaceus fruiting body had less significant protective and restorative effects on the brain cells of zebrafish embryos. Both the ethanol and hot water extracts from H. erinaceus solid-state fermented wheat product could protect and repair the brain cells of zebrafish embryos damaged by 1% ethanol. Therefore, it has great potential as a raw material for neuroprotective health product.

Practice Parameter: Management of Hyperbilirubinemia in the Healthy Term Newborn

PEDIATRICS ◽  
1994 ◽  
Vol 94 (4) ◽  
pp. 558-565
Author(s):  
◽  
Keyword(s):  
Serum Bilirubin ◽  
Elevated Serum ◽  
The United States ◽  
Total Serum ◽  
Brain Cells ◽  
Albumin Concentration ◽  
Specific Level ◽  
Term Newborn ◽  
Term Newborns ◽  
The Brain

Each year approximately 60% of the 4 million newborns in the United States become clinically jaundiced. Many receive various forms of evaluation and treatment. Few issues in neonatal medicine have generated such long-standing controversy as the possible adverse consequences of neonatal jaundice and when to begin treatment. Questions regarding potentially detrimental neurologic effects from elevated serum bilirubin levels prompt continuing concern and debate, particularly with regard to the management of the otherwise healthy term newborn without risk factors for hemolysis. Although most data are based on infants with birth weights ≥2500 g, "term" is hereafter defined as 37 completed weeks of gestation. Under certain circumstances, bilirubin may be toxic to the central nervous system and may cause neurologic impairment even in healthy term newborns. Most studies, however, have failed to substantiate significant associations between a specific level of total serum bilirubin (TSB) during nonhemolytic hyperbilirubinemia in term newborns and subsequent IQ or serious neurologic abnormality (including hearing impairment). Other studies have detected subtle differences in outcomes associated with TSB levels, particularly when used in conjunction with albumin binding tests and/or duration of exposure. In almost all published studies, the TSB concentration has been used as a predictor variable for outcome determinations. Factors influencing bilirubin toxicity to the brain cells of newborn infants are complex and incompletely understood; they include those that affect the serum albumin concentration and those that affect the binding of bilirubin to albumin, the penetration of bilirubin into the brain, and the vulnerability of brain cells to the toxic effects of bilirubin.

The brain cells that help animals navigate in 3D

Nature ◽  
2021 ◽  
Author(s):  
Benjamin Thompson ◽  
Nick Petrić Howe
Keyword(s):  
Brain Cells ◽  
The Brain

scholarly journals Coenzyme Q10 and its effects in the treatment of neurodegenerative diseases

2009 ◽  
Vol 45 (4) ◽  
pp. 607-618 ◽  
Author(s):  
Graciela Cristina dos Santos ◽  
Lusânia Maria Greggi Antunes ◽  
Antonio Cardozo dos Santos ◽  
Maria de Lourdes Pires Bianchi
Keyword(s):  
Neurodegenerative Diseases ◽  
Health Risks ◽  
Coenzyme Q10 ◽  
Cellular Respiration ◽  
Irreversible Loss ◽  
Beneficial Effects ◽  
Pathological Conditions ◽  
Electron Transportation ◽  
The Brain ◽  
Lateral Sclerosis

According to clinical and pre-clinical studies, oxidative stress and its consequences may be the cause or, at least, a contributing factor, to a large number of neurodegenerative diseases. These diseases include common and debilitating disorders, characterized by progressive and irreversible loss of neurons in specific regions of the brain. The most common neurodegenerative diseases are Parkinson's disease, Huntington's disease, Alzheimer's disease and amyotrophic lateral sclerosis. Coenzyme Q10 (CoQ10) has been extensively studied since its discovery in 1957. It is a component of the electron transportation chain and participates in aerobic cellular respiration, generating energy in the form of adenosine triphosphate (ATP). The property of CoQ10 to act as an antioxidant or a pro-oxidant, suggests that it also plays an important role in the modulation of redox cellular status under physiological and pathological conditions, also performing a role in the ageing process. In several animal models of neurodegenerative diseases, CoQ10 has shown beneficial effects in reducing disease progression. However, further studies are needed to assess the outcome and effectiveness of CoQ10 before exposing patients to unnecessary health risks at significant costs.

The use of siRNA as a pharmacological tool to assess a role for the transcription factor NF-IL6 in the brain under in vitro and in vivo conditions during LPS-induced inflammatory stimulation

2017 ◽  
Vol 28 (6) ◽  
Author(s):  
Jelena Damm ◽  
Joachim Roth ◽  
Rüdiger Gerstberger ◽  
Christoph Rummel
Keyword(s):  
Transcription Factor ◽  
Brain Cells ◽  
Nuclear Factor ◽  
Si Rna ◽  
The Brain ◽  
Deficient Mice ◽  
Transcription Factor Nuclear Factor

AbstractBackground:Studies with NF-IL6-deficient mice indicate that this transcription factor plays a dual role during systemic inflammation with pro- and anti-inflammatory capacities. Here, we aimed to characterize the role of NF-IL6 specifically within the brain.Methods:In this study, we tested the capacity of short interfering (si) RNA to silence the inflammatory transcription factor nuclear factor-interleukin 6 (NF-IL6) in brain cells underResults:In cells of a mixed neuronal and glial primary culture from the ratConclusions:This approach was, thus, not suitable to characterize the role NF-IL6 in the brain

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